Role for thromboxane receptors in angiotensin-II-Induced hypertension
Role for thromboxane receptors in angiotensin-II-Induced hypertension
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DOI：
10.1161/01.hyp.0000112225.27560.24
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发表时间：
2004-02-01
期刊：
影响因子：
8.3
通讯作者：
Coffman, TM
中科院分区：
文献类型：
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作者：
Francois, H;Athirakul, K;Coffman, TM
为了评估血栓素在高血压及其并发症中的作用，我们研究了在血管紧张素-II 依赖性高血压模型中靶向破坏 TXA2 受体基因的小鼠。为了确定遗传背景是否可能改变 TP 受体的生理作用，我们研究了两个具有不同遗传背景的 TP 敲除 (Tp(-/-)) 小鼠系（C57BL/6 和 BALB/c）。在慢性血管紧张素 II 输注期间（通过皮下渗透泵每分钟 1000 ng/kg x 28 天），TP 缺乏可以防止 C57BL/6 背景的死亡，但不能防止 BALB/c 菌株的死亡。长期输注血管紧张素 II 还会导致野生型 (WT) C57BL/6 和 BALB/c 动物的血压快速显着升高，而在任一背景下的 Tp(-/-) 小鼠中血压显着减弱。输注28天后，仅C57BL/6品系出现心脏肥大：WT小鼠的心脏/体重比增加了57%+/-8%，而Tp(-/-)小鼠的心脏/体重比增加了17%+/-6.5%（P
To evaluate the role of thromboxane in hypertension and its complications, we studied mice with targeted disruption of the TXA2 receptor gene in an angiotensin-II-dependent model of hypertension. To determine whether genetic background might alter the physiological actions of the TP receptor, we studied two lines of TP knockout (Tp(-/-)) mice with distinct genetic backgrounds (C57BL/6 and BALB/c). During chronic angiotensin II infusion (1000 ng/kg per minute x 28 days by subcutaneous osmotic pump), TP deficiency prevented mortality in the C57BL/6 background but not in the BALB/c strain. Chronic angiotensin II infusion also caused a rapid and significant increase in blood pressure in wild-type (WT) C57BL/6 and BALB/c animals, which was significantly attenuated in Tp(-/-) mice on either background. After 28 days of infusion, cardiac hypertrophy only occurred in the C57BL/6 strain: heart/body weight ratio increased by 57%+/-8% in WT mice compared with 17%+/-6.5% for the Tp(-/-) mice (P